The GSK3β pathway in optic nerve regeneration

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Adult neurons in the mammalian central nervous system (CNS) fail to regenerate after injury due to a number of factors including the reduced intrinsic growth capacity together with the hostile environment of the injured CNS microenvironment [1-4]. However recent studies have shown that modifying the intrinsic growth capacity through a number of cell signalling pathways can promote regeneration of adult CNS neurons. For example, intrinsic factors such as cyclic adenosine monophosphate (cAMP), mammalian target of rapamycin (mTOR), and the repressors phosphatase and tensin homolog (PTEN) and suppressor of cytokine signalling 3 (SOCS3) promote CNS axon regeneration [5-7]. The observation that cAMP and mTOR activity are developmentally downregulated and new protein synthesis is suppressed after mTOR inactivation probably explains why some axons do not normally regenerate in the mature CNS.
Original languageEnglish
Pages (from-to)10-16
Number of pages7
JournalArchives of Clinical and Experimental Ophthalmology
Issue number1
Publication statusPublished - 14 Jul 2020


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